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N6-methyladenosine modifications in maternal-fetal crosstalk and gestational diseases.
Wu, Suqi; Liu, Ketong; Zhou, Bingyan; Wu, Suwen.
Afiliación
  • Wu S; First Clinical Medical College, Zhejiang Chinese Medical University, Hangzhou, China.
  • Liu K; Department of Obstetrics, Obstetrics and Gynecology Hospital of Fudan University, Shanghai, China.
  • Zhou B; Hubei Clinical Center of Hirschsprung's Disease and Allied Disorders, Department of Pediatric Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
  • Wu S; Department of Obstetrics, Obstetrics and Gynecology Hospital of Fudan University, Shanghai, China.
Front Cell Dev Biol ; 11: 1164706, 2023.
Article en En | MEDLINE | ID: mdl-37009476
ABSTRACT
As a medium among pregnant women, environment and fetus, placenta owns powerful and delicate epigenetic processes to regulate gene expression and maintain cellular homeostasis. N6-methyladenosine (m6A) is the most prevalent modification that determines the fate of RNA, and its dynamic reversibility indicates that m6A may serve as a sensitive responder to environmental stimuli. Emerging evidence suggests that m6A modifications play an essential role in placental development and maternal-fetal crosstalk, and are closely related to gestational diseases. Herein, we summarized the latest techniques for m6A sequencing and highlighted current advances of m6A modifications in maternal-fetal crosstalk and the underlying mechanisms in gestational diseases. Therefore, proper m6A modifications are important in placental development, but its disturbance mainly caused by various environmental factors can lead to abnormal placentation and function with possible consequences of gestational diseases, fetal growth and disease susceptibility in adulthood.
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Texto completo: 1 Bases de datos: MEDLINE Idioma: En Revista: Front Cell Dev Biol Año: 2023 Tipo del documento: Article País de afiliación: China

Texto completo: 1 Bases de datos: MEDLINE Idioma: En Revista: Front Cell Dev Biol Año: 2023 Tipo del documento: Article País de afiliación: China